About: Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo
Creator	Rottier, Peter Raaben, Matthijs Ja, Marian Koerkamp, Groot
Source	Medline; PMC
abstract	BACKGROUND: The role of type I IFNs in protecting against coronavirus (CoV) infections is not fully understood. While CoVs are poor inducers of type I IFNs in tissue culture, several studies have demonstrated the importance of the type I IFN response in controlling MHV infection in animals. The protective effectors against MHV infection are, however, still unknown. RESULTS: In order to get more insight into the antiviral gene expression induced in the brains of MHV-infected mice, we performed whole-genome expression profiling. Three different mouse strains, differing in their susceptibility to infection with MHV, were used. In BALB/c mice, which display high viral loads but are able to control the infection, 57 and 121 genes were significantly differentially expressed (≥ 1.5 fold change) upon infection at 2 and 5 days post infection, respectively. Functional association network analyses demonstrated a strong type I IFN response, with Irf1 and Irf7 as the central players. At 5 days post infection, a type II IFN response also becomes apparent. Both the type I and II IFN response, which were more pronounced in mice with a higher viral load, were not observed in 129SvEv mice, which are much less susceptible to infection with MHV. 129SvEv mice lacking the type I interferon receptor (IFNAR-/-), however, were not able to control the infection. Gene expression profiling of these mice identified type I IFN-independent responses to infection, with IFN-γ as the central player. As the BALB/c and the IFNAR-/- 129SvEv mice demonstrated very similar viral loads in their brains, we also compared their gene expression profiles upon infection with MHV in order to identify type I IFN-dependent transcriptional responses. Many known IFN-inducible genes were detected, several of which have previously been shown to play an important protective role against virus infections. We speculate that the additional type I IFN-dependent genes that we discovered may also be important for protection against MHV infection. CONCLUSION: Transcriptional profiling of mice infected with MHV demonstrated the induction of a robust IFN response, which correlated with the viral load. Profiling of IFNAR-/- mice allowed us to identify type I IFN-independent and -dependent responses. Overall, this study broadens our present knowledge of the type I and II IFN-mediated effector responses during CoV infection in vivo.
has issue date	2009-08-03(xsd:dateTime)
bibo:doi	10.1186/1471-2164-10-350
bibo:pmid	19650917
has license	cc-by
sha1sum (hex)	0953fa36903063f60627e07f7b4e07f0aec3c4d3
schema:url	https://doi.org/10.1186/1471-2164-10-350
resource representing a document's title	Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo
has PubMed Central identifier	PMC2728740
has PubMed identifier	19650917
schema:publication	BMC Genomics
resource representing a document's body	covid:0953fa36903063f60627e07f7b4e07f0aec3c4d3#body_text
is schema:about of	named entity 'animals' named entity 'While' named entity 'type I IFNs' named entity 'infection' named entity 'vivo' named entity 'ANIMALS' named entity 'CORONAVIRUS' named entity 'UNDERSTOOD' named entity 'PROTECTING' named entity 'INFECTION' named entity 'POOR' named entity 'RESPONSE' named entity 'DEMONSTRATED' named entity 'HAVE' named entity 'CONTROLLING' named entity 'INDEPENDENT' covid:arg/0953fa36903063f60627e07f7b4e07f0aec3c4d3 named entity 'TYPE I INTERFERON RECEPTOR' named entity 'MOUSE HEPATITIS' named entity 'HOST' named entity 'DEPENDENT' named entity 'TRANSCRIPTIONAL' named entity 'RESPONSES' named entity 'GENOMICS' named entity 'BMC' named entity 'CORONAVIRUS INFECTION' named entity 'INFECTIONS' named entity 'TISSUE CULTURE' named entity 'IFN' named entity 'MHV' named entity 'COVS' named entity 'IN VIVO' named entity 'FULLY' named entity 'ROLE' named entity 'STUDIES' named entity 'TYPE I' named entity 'UNKNOWN' named entity 'inducers' named entity 'controlling' named entity 'transcriptional' named entity 'type I IFNs' named entity 'coronavirus infection' named entity 'receptor' named entity 'IFNAR' named entity 'Ctss' named entity 'intraperitoneal' named entity 'type I IFNs' named entity 'mice' named entity 'inoculation' named entity 'mice' named entity 'microarray' named entity 'liver' named entity 'IFNAR' named entity 'ethics committee' named entity 'infection' named entity 'double-stranded RNA' named entity 'isoforms' named entity 'transcriptional' named entity 'virus replication' named entity 'mice' named entity 'type I IFN' named entity 'type I IFN' named entity 'viral RNA' named entity 'reverse transcriptase' named entity 'type I IFN' named entity 'A59' named entity 'mice' named entity 'inoculation' named entity 'TaqMan' named entity 'infection' named entity 'viral RNA' named entity 'esters' named entity 'infection' named entity 'mice' named entity 'mRNA' named entity 'RNA' named entity 'mice' named entity 'gene expression'

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